Tricuspid stenosis

Overview

•Rare valvular lesion causing obstruction to right ventricular inflow during diastole → right atrial hypertension → systemic venous congestion

•Most common cause: rheumatic heart disease (almost always with concurrent mitral stenosis)

•Carcinoid syndrome - circulating serotonin causes fibrous plaques on right-sided valves; tricuspid stenosis + pulmonary stenosis are characteristic; left-sided valves spared (liver inactivates mediators) unless hepatic metastases

•Congenital tricuspid stenosis - extremely rare; Ebstein's anomaly primarily causes regurgitation not stenosis

Presentation

•Features of systemic venous congestion: raised JVP (prominent 'a' wave), peripheral oedema, hepatomegaly, ascites

•Breathlessness and pulmonary oedema notably absent or mild - key clinical clue (right ventricle protected from excess output)

•Murmur: mid-late diastolic, low-pitched, rumbling; heard best at left lower sternal border (4th intercostal space, left parasternal)

•Louder on inspiration (Carvallo's sign) - applies to all right-sided murmurs

•Opening snap may be present after S2

💡

Mitral stenosis without the expected degree of pulmonary congestion should prompt consideration of co-existing tricuspid stenosis reducing right heart output.

🎯

Tricuspid stenosis vs tricuspid regurgitation: both are loudest at the left lower sternal border and increase on inspiration - but tricuspid stenosis is a diastolic murmur, tricuspid regurgitation is a pan-systolic murmur.

Investigations

🥇 First-line

•transthoracic echocardiography - valve area (severe <1.0 cm²), mean pressure gradient (significant >5 mmHg), right atrial enlargement

•ECG - right atrial enlargement: tall, peaked P waves >2.5 mm in lead II ('P pulmonale'); may show atrial fibrillation

•Chest X-ray - right atrial enlargement; absence of pulmonary venous congestion (distinguishes from mitral stenosis)

🏆 Gold standard

•cardiac catheterisation - directly measures trans-tricuspid pressure gradient; used when echo is inconclusive or prior to intervention

•If carcinoid suspected: urinary 5-HIAA and serum chromogranin A

Management

•First-line (symptomatic relief): furosemide + spironolactone - reduce systemic venous congestion; avoid excessive preload reduction

•Anticoagulation: warfarin - if atrial fibrillation present (enlarged right atrium → high thromboembolic risk)

🥈 Second-line

•percutaneous balloon tricuspid valvuloplasty - for pliable, non-calcified (rheumatic) valves; performed alongside mitral valvuloplasty if both valves affected

🥉 Third-line

•surgical repair (commissurotomy) or valve replacement - if calcified, concurrent regurgitation, or open-heart surgery needed; bioprosthetic valves preferred (mechanical prostheses have high thrombosis rates in tricuspid position)

•Carcinoid-associated disease: octreotide (somatostatin analogue) slows progression; surgical valve replacement ultimately required for symptomatic disease

Complications

•Atrial fibrillation - right atrial dilatation; increases thromboembolic risk

•Cardiac cirrhosis - chronic hepatic venous congestion → centrilobular necrosis and fibrosis

•Right heart failure - end-stage consequence

•Post-valvuloplasty tricuspid regurgitation - recognised complication of balloon valvuloplasty